{"id":14661,"date":"2020-09-24T20:15:25","date_gmt":"2020-09-24T18:15:25","guid":{"rendered":"https:\/\/idibell.cat\/en\/?p=14661"},"modified":"2020-09-23T12:13:17","modified_gmt":"2020-09-23T10:13:17","slug":"interferon-the-key-to-many-of-the-worst-cases-of-covid-19-in-young-people","status":"publish","type":"post","link":"https:\/\/idibell.cat\/en\/2020\/09\/interferon-the-key-to-many-of-the-worst-cases-of-covid-19-in-young-people\/","title":{"rendered":"Interferon, the key to many of the worst cases of COVID-19 in young people"},"content":{"rendered":"
Age, sex, and the presence of previous pathologies are the main factors associated with a worse prognosis for COVID-19, but the causes that lead young people without comorbidities to develop severe forms of the disease are still unknown. In two articles published today in the journal Science<\/strong> <\/em>and with the participation of Dr. Aurora Pujol, geneticist and ICREA professor at the Bellvitge Biomedical Research Institute (IDIBELL<\/a>), researchers identify alterations of interferon and the proteins of its signalling pathway as predictive markers of severity in these individuals<\/strong>.<\/p>\n The international consortium Covid Human Genetic Effort<\/strong><\/a>, led by the Rockefeller University of New York, has analysed the genomes of 659 severe COVID-19 patients and has found a high frequency of mutations that would affect the levels of interferon and the proteins of the lung cells responsible for its activity. Specifically, genetic alterations have been detected in eight genes<\/strong> important in the immune response against viruses, while a similar group of asymptomatic or mild patients did not have these mutations.<\/p>\n Knowing the importance of these alterations in the evolution of the disease can become an important therapeutic and preventive tool since it will be very useful for the selection of the population at risk of developing severe pneumonia, which will facilitate the screening<\/strong> of patients who require a special care and priority access to artificial ventilation or the ICU. \u201cNow that we know one of the molecular causes of why some young people develop severe forms of the disease, we can fine-tune our therapeutic options, such as interferon treatment,<\/em>\u201d adds Pujol.<\/p>\n \u201cNow that we know one of the molecular causes of why some young people develop severe forms of the disease, we can fine-tune our therapeutic options, such as interferon treatment<\/em>\u201d<\/p><\/blockquote>\n This list of mutations, which could also be relevant in other viruses, is likely to expand as more cases are studied. “COVID-19 patients with a worse prognosis who do not have any of these alterations may have a previous undiagnosed pathology or other genetic susceptibilities that cause an incorrect immune response<\/em>,” explains Pujol.<\/p>\n Interferons<\/strong> are hormone-like signalling proteins that are essential in the body defence against viral infections. This type of immune response is even more important in the fight against the SARS-CoV-2 virus, since the virus itself has mechanisms to reduce the production of interferon by the cells of the immune system. Therefore, in people with these mutations, the effects would add up and the virus would go unnoticed by the body’s defences.<\/p>\n The results are the fruit of a collaboration between hundreds of hospitals that were collecting samples in the harshest moments of the first wave of the pandemic and of researchers who have sequenced and analysed the data even from the lockdown. Apart from IDIBELL, this study has also had the participation of specialists from the Vall d’Hebron Research Institute (VHIR<\/a>).<\/p>\n On the other hand, the National Center for Genomic Analysis (CNAG-CRG<\/a>) was in charge of analyzing the genome of COVID-19 patients through the EU-funded project EASI-Genomics, which is coordinated by CNAG-CRG. The unit led by Marta Gut offered a new generation clinical grade sequencing with rapid response that is essential in a pandemic<\/p>\n <\/p>\n <\/p>\nAutoantibodies against interferon<\/h3>\n